POSTTRAUMATIC STRESS DISORDER AND METABOLISM
Pedro Correia1, 2, Eszter Sipos1, Flóra Bek-Balla1, Csilla Fazekas1, 2, Bibiána Török1, 2, Dóra Zelena1, 3
People exposed to a traumatic event can develop posttraumatic stress disorder (PTSD). This disorder is a devastating condition with various symptoms including hyperarousal, recollection of the trauma, concentration problems and social isolation. Previous studies showed that PTSD is often co-morbid with other disorders, especially with metabolic diseases. The aim of this study is to identify the development of metabolic alterations caused by traumatic events for better understanding of the pathophysiology of PTSD and further promote effective treatments for these comorbidities. During this study, PTSD was induced by electric footshock in rats and the metabolic changes were followed by a Metabolic Research Platform. Those changes were not only measured right after the trauma, but also 2 and 4 weeks after it. In agreement with the comfort food theory of Mary Dallman, the acute stress of footshock led to elevated food intake. However, in the long run, trauma led to a decreased food intake and locomotion, reflecting an anhedonic phenotype. Moreover, it was also observed that only acute reminders of the shock led to an enhanced food consumption without accompanied elevation of energy utilisation, which might lead- if happens repeatedly- to development of obesity. Thus, our results suggest that it is necessary to use constant reminders of the trauma to accurately analyse comorbidity, because, without them, we were not able to detect any changes in the body weight or blood sugar level of this animal model.